| First Author | Bombardier E | Year | 2013 |
| Journal | FASEB J | Volume | 27 |
| Issue | 9 | Pages | 3871-8 |
| PubMed ID | 23752204 | Mgi Jnum | J:201178 |
| Mgi Id | MGI:5511116 | Doi | 10.1096/fj.13-230631 |
| Citation | Bombardier E, et al. (2013) Sarcolipin trumps beta-adrenergic receptor signaling as the favored mechanism for muscle-based diet-induced thermogenesis. FASEB J 27(9):3871-8 |
| abstractText | Sarcolipin (SLN) regulates muscle-based nonshivering thermogenesis and is up-regulated with high-fat feeding (HFF). To investigate whether other muscle-based thermogenic systems compensate for a lack of Sln and to firmly establish SLN as a mediator of diet-induced thermogenesis (DIT), we measured muscle and whole-body energy expenditure in chow- and high-fat-fed Sln(-/-) and wild-type (WT) mice. Following HFF, resting muscle metabolic rate (Vo2, mul/g/s) was increased similarly in WT (0.28+/-0.02 vs. 0.31+/-0.03) and Sln(-/-) (0.23+/-0.03 vs. 0.35+/-0.02) mice due to increased sympathetic nervous system activation in Sln(-/-) mice; however, whole-body metabolic rate (Vo2, ml/kg/h) was lower in Sln(-/-) compared with WT mice following HFF but only during periods when the mice were active in their cages (WT, 2894+/-87 vs. Sln(-/-), 2708+/-61). Treatment with the beta-adrenergic receptor (beta-AR) antagonist propranolol during HFF completely prevented muscle-based DIT in Sln(-/-) mice; however, it had no effect in WT mice, resulting in greater differences in whole-body metabolic rate and diet-induced weight gain. Our results suggest that beta-AR signaling partially compensates for a lack of SLN to activate muscle-based DIT, but SLN is the primary and more effective mediator.-Bombardier, E., Smith, I. C., Gamu, D., Fajardo, V. A., Vigna, C., Sayer, R. A., Gupta, S. C., Bal, N. C., Periasamy, M., Tupling, A. R. Sarcolipin trumps beta-adrenergic receptor signaling as the favored mechanism for muscle-based diet-induced thermogenesis. |
